Abstract: Galphimia glauca is a plant species that has been used in mexican traditional Medicine for the treatment of central nervous system disorders. It was demonstrated that the standardized extract of G. glauca, by means of double-blind, controlled and randomized clinical studies, possesses therapeutic effectiveness in patients with generalized anxiety disorder. In the active extract, nor-secotriterpenes Galphimines, Galphimine-A (G-A) and Galphimine-B (G-B) are prominent for their anxiolytic effect. In the present work, the oral administration of different doses of G-A in ICR male mice submitted to the Elevated Plus Maze (EPM) test was capable of inducing a significant anxiolytic effect, while any of the doses modified the spontaneous motor activity of the mice in the Open Field Test (OFT). The administration of G-A (30 mg kg1, p.o.) in mice inhibited the anxiogenic effect of picrotoxin (PTX, 2 mg kg1, i.p.), but not of bicuculline (BCC, 5 mg kg1, i.p.) and pentylenetetrazole (PTZ, 10 mg kg1, i.p.) in the EPM. The combination of G-A with these drugs was evaluated by means of in vivo extracellular recordings in basolateral amygdala (BLA). A dose-dependent increase of the firing rate on BLA neurons was induced by the administration (i.v.) of different doses of G-A, while diazepam (DZP) decreased the firing rate. The co-administration of G-A with DZP or flumazenil (FMZ) did not modify the effect produced by these drugs on the firing rate. However, the co-administration of G-A modified the effect produced by PTX. The G-A was able to produce an anxiolytic effect when administered at different doses orally in mice, without inducing an associated sedative effect. Electrophysiological recordings showed that the effect produced by G-A is different of that of DZP and suggest that G-A do not interact directly with the GABAergic system (transmission mechanism for the g-aminobutyric acid-GABA), while it was able to modify the effect produced by PTX, BCC and Phaclofen evidencing a different action mechanism.